• Biomolecules & Therapeutics
• /
• v.3 no.4
• /
• pp.304-310
• /
• 1995

This study was done to investigate the effect of vitamin C on hepatic biliary and microsomal function during ischemia and reperfusion. Rats were treated with vitamin C(20, 100, 400, 1600 mg/kg) or with vehicle(saline) and then subjected to 60 min no-flow hepatic ischemia in vivo. Control animals were time-matched sham ischemic animals. After 1 or 5 hr of reperfusion, bile was collected, blood was obtained from the abdominal aorta, and liver microsomes were isolated. In vehicle-treated ischemic rats, serum ALT and AST levels peaked at 5 hr and were significantly attenuated by vitamin C 20 mg/kg and 100 mg/kg treatment. Similarly, hepatic wet weight-to-dry weight ratio was decreased in the vehicle-treated ischemic group. Vitamin C 20 mg/kg and 100 mg/kg treatment minimized the increase in this ratio. Lipid peroxidation was elevated in vehicle-treated ischemic group, but this elevation was also inhibited by vitamin C 20 mg/kg and 100 mg/kg treatment. Bile flow and cholate output, but not bilirubin output, were markedly decreased by ischemia/reperfuzion. Vitamin C 20 mg/kg and 100mg/kg treatment restored the secretion but vitamin C 1600 mg/kg reduced the cholate output. Cytochrome P-450 content was decreased by ischemia/reperfusion and restored by vitamin C 20 mg/kg and 100 mg/kg treatment to the level of sham operated group but decreased by vitamin C 1600 mg/kg. Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase activity was increased by ischemia/reperfusion. The changes in the activities of aminopyrine were prevented by vitamin C 20 mg/kg and 100 mg/kg treatment, but not by 400 mg/kg and 1600 mg/kg treatment. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions as well as microsomal drug metabolizing systems, small doses(20, 100 mg/kg) of vitamin C significantly ameliorates and large doses(400, 1600 mg/kg) of vitamin C aggravated these ischemia/reperfusion-induced changes.

• Preventive Nutrition and Food Science
• /
• v.3 no.4
• /
• pp.344-350
• /
• 1998

Lipid lowering properties from three plant water extracts, Rosa rugosa, Crataegus pinnatifida and Polygonum cuspidatum, were tested by supplementing a 1% high-cholesterol diet with them in rats. Plasma triglyceride levels in Rosa fugosa, Crataegus pinnatifida and Polygonum cuspidatum groups were significantly lower compared to that of the control. by 29% , 24% and 47% respectively. hepatic trigylceride levels in Rosa rugosa and Crataegus pinnatifida groups were significantly lower compared to the control by 11% and 15% respectively. Hepatic HMG-CoA reductase activity in Rosa rugosa group was significantly greater compared to the control by 406%. Hepatic ACAT activity was significantly lower in Polygonum cuspidatum group compared to the control by 28%. by multiple regression results, only plasma cholesterol was associated significantly (p<0.05) with liver HMG-CoA reductase activity. Plasma cholesterol explained 12% of thevariance of the liver HMG-CoA redctase activity. In conclusion, we have showen that hot water extracts from Rosa rugosa, Crataegus pinnatifida and Polygonum cuspidatum lowered plasma triglycerides in rats fed on a high-cholesterol diet. Data suggests that these extracts could potentially prevent or treat hypertriglyceridemia induced by a high fat diet and fatty liver.

• Journal of Veterinary Clinics
• /
• v.33 no.3
• /
• pp.160-164
• /
• 2016

A Turkish angora cat with a one-week history of anorexia and vomiting was diagnosed with hepatic lipidosis. During hospitalization and treatment, the cat suddenly showed respiratory-related clinical signs, including coughing and dyspnea, 13 days after initial diagnosis. Due to the poor response to treatment, the patient was euthanized at the owner's request. A postmortem histopathologic examination of the cat's heart showed dilation and wall thinning of the right atrium and ventricle, with fibrofatty infiltration corresponding to an arrhythmogenic right ventricular cardiomyopathy (ARVC). This is a case report of ARVC concurrent with hepatic lipidosis in a cat; both diseases are related to disturbances in lipid metabolism.

• Proceedings of the Ginseng society Conference
• /
• 1987.06a
• /
• pp.47-58
• /
• 1987

Ethanol exerts different effects on hepatic cellular metabolism, depending mainly on the duration of its intake. In the presence of ethanol following an acute load, a number of hepatic functions are inhibited, including lipid oxidation and microsomal drug metabolism. In its early stages, chronic ethanol consumption produces adaptive metabolic changes in the endoplasmic reticulum which result in increased metabolism of ethanol and drugs and accelerated lipoprotein production. Prolongation of ethanol intake may result in injurious hepatic lesions such as alcoholic hepatitis and cirrhosis A number of such metabolic effects of ethanol are directly linked to the two major products of its oxidation; hydrogen and acetaldehyde. The excess hydrogen from ethanol unbalances the liver cell's chemistry. In the presence of excess hydrogen ions the process is turned in a different direction. In this study, it was attempted to observe the effect of ginseng saponins on alcohol Oehydrogenase(ADH), aldehyde dehydrogenase(ALDH) and microsomal ethanol oxidizing system(MEOS) in vivo as well as in vitro. Furthermore, the effect of ginseng saponin on the hydrogen balance in the liver and the hepatic cellular distribution of (1-14C) ethanol, its incorporation into acetaldehyde and lipids was also investigated. It seemed that ginseng saponin stimulated the above enzymes and other related enzymes in ethanol metabolism, resulting in a rapid removal of acetaldehyde and excess hydrogen from the animal body,

• Journal of Nutrition and Health
• /
• v.40 no.4
• /
• pp.295-302
• /
• 2007

This study was designed to examine the effects of fractions of ethanol extract of Benincasa hispida (wax gourd) on hepatic antioxidative status in streptozotocin (STZ) induced diabetic rats. Sprague-Dawley rats were induced diabetes mellitus by STZ injection (45 mg/kg) into the tail vein and were divided into 5 groups: normal, STZ-control, three experimental diabetic groups. Fractions of ethanol extract of Benincasa hispida were administered orally into the diabetic rats for 14 days. Hepatic glutathione peroxidase (GSH-px) activity (determined with H$_2$O$_2$ as substrate) was increased in the groups supplemented with chloroform (CHCl$_3$) and butanol (BuOH) fractions. Glutathione peroxidase (GR) activity in the liver cytosol of H$_2$O fraction groups was significantly lower than that of STZ-control group. The H$_{2}$O fraction supplemented group has been shown the notably decrease in the hepatic superoxide dismutase (SOD) activity. The hepatic cytosol catalase (CAT) activity was significant decreased by the supplementation with BuOH fraction. It was found from the results that the supplementation of BuOH and H$_2$O fractions of Benincasa hispida extract could be beneficial for the diabetic complications and damages from the lipid peroxidation.

• Korean Journal of Community Nutrition
• /
• v.9 no.4
• /
• pp.536-544
• /
• 2004

To evaluate the antioxidative effect of maengjong-juk (Phyllostachys pubescens) extract coated rice in vivo system, maengjong-juk extract coated rice diets were fed to C57BL/6 mice for 16 weeks. Plasma total antioxidative capacity, hepatic lipid peroxidation, protein oxidation, activities of antioxidative enzymes and total glutathione content were measured. Plasma total antioxidative capacity was elevated significantly in maengjong-juk extract diets supplemented group in a dose dependant manner. Hepatic TBARS contents were significantly decreased in maengjong-juk extract diets supplemented group compared to high cholesterol group. Maengjong-juk extract coated rice diets suppressed the protein oxidation significantly in liver. Activities of hepatic antioxidative enzymes such as total SOD, CuㆍZn-SOD, Mn-SOD, GSH-Px and catalase activities of maengjong-juk extract coated rice diets were significantly higher than those of high cholesterol diet. Total hepatic glutathione content was significantly increased by maengjong-juk extract coated rice diets administration. According to this study, numerous antioxidative materials and phytochemicals containing in maengjong-juk extracts appear to protect antioxidative systems in C57BL/6 mice fed bamboo extract coated rice diet. (Korean J Community Nutrition 9(4): 536∼544, 2004)

• Archives of Pharmacal Research
• /
• v.27 no.2
• /
• pp.184-188
• /
• 2004

The present study was carried out to clarify whether tectorigenin and tectoridin isolated from the rhizomes of Belamcanda chinensis (Iridaceae) inhibit hepatic damage induced by carbon tetrachloride ($CCl_4$)-intoxication in rats by the experimental methods in vitro and in vivo. Tectorigenin and tectoridin exhibited a significant decrease in serum transaminase activities elevated by hepatic damage induced by $CCl_4$-intoxication in rats, as well as in a lipid peroxidation causing a significant decrease in malondialdehyde (MDA) production by thiobarbituric acid (TBA)-reactant assay. Both compounds also showed strong increase in the antioxidant enzymes such as hepatic cytosolic superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-px) activities in $CCl_4$-intoxicated rats. These results suggested that tectorigenin and tectoridin isolated from the rhizomes of B. chinensis possess not only the antioxidative, but also the hepatoprotective activities in $CCl_4$ -intoxicated rats.

• Food Science and Biotechnology
• /
• v.15 no.4
• /
• pp.612-616
• /
• 2006

The protective effect of water extract of ash tree leaves (ALE) against oxidative damages was investigated in paracetamol-induced BALB/c mice. Biochemical analysis of anti-oxidative enzymes, immunoblot analyses of hepatic cytochrome P450 2El (CYP2E1), and the gene expression of tumor necrosis factor (TNF-${\alpha}$) were examined to determine the extract's protective effect and its possible mechanisms. BALB/c mice were divided into three groups: normal, paracetamol-administered, and ALE-pretreated groups. A single dose of paracetamol led to a marked increase in lipid peroxidation as measured by malondialdehyde (MDA). This was associated with a significant reduction in the hepatic antioxidant system, e.g., glutathione (GSH). Paracetamol administration also significantly elevated the expression of CYP2E1, according to immunoblot analysis, and of TNF-${\alpha}$ mRNA in liver. However, ALE pretreatment prior to the administration of paracetamol significantly decreased hepatic MDA levels. ALE restored hepatic glutathione and catalase levels and suppressed the expression of CYP2E1 and TNF-${\alpha}$ observed in inflammatory tissues. Moreover, ALE restored mitochondrial ATP content depleted by the drug administration. These results show that the extract of ash tree leaves protects against paracetamol-induced oxidative damages by blocking oxidative stress and CYP2E1-mediated paracetamol bioactivation.

• Archives of Pharmacal Research
• /
• v.28 no.12
• /
• pp.1392-1399
• /
• 2005

This study evaluated the effect of $\alpha$-tocopherol ($\alpha$-TC), ischemic preconditioning (IPC) or a combination on the extent of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R). Rats were pretreated with $\alpha$-TC (20 mg/kg per day, i.p.) for 3 days before sustained ischemia. A rat liver was preconditioned with 10 min of ischemia and 10 min of reperfusion, and was then subjected to 90 min of ischemia followed by 5 h or 24 h of reperfusion. I/R increased the aminotransferase activity and mitochondrial lipid peroxidation, whereas it decreased the mitochondrial glutamate dehydrogenase activity. $\alpha$-TC and IPC individually attenuated these changes. $\alpha$-TC combined with IPC ($\alpha$-TC+IPC) did not further attenuate the changes. The mitochondrial glutathione content decreased after 5 h reperfusion. This decrease was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The significant production of peroxides observed after 10 min reperfusion subsequent to sustained ischemia was attenuated by $\alpha$-TC, IPC, and $\alpha$-TC+IPC. The mitochondria isolated after I/R were rapidly swollen. However, this swelling rate was reduced by $\alpha$­TC, IPC, and $\alpha$-TC+IPC. These results suggest that either $\alpha$-TC or IPC reduces the level of mitochondrial damage associated with oxidative stress caused by hepatic I/R, but $\alpha$- TC combined with IPC offers no significant additional protection.

• Molecules and Cells
• /
• v.44 no.2
• /
• pp.116-125
• /
• 2021

Cardiovascular diseases (CVDs) are the most common cause of death in patients with nonalcoholic fatty liver disease (NAFLD) and dyslipidemia is considered at least partially responsible for the increased CVD risk in NAFLD patients. The aim of the present study is to understand how hepatic de novo lipogenesis influences hepatic cholesterol content as well as its effects on the plasma lipid levels. Hepatic lipogenesis was induced in mice by feeding a fat-free/high-sucrose (FF/HS) diet and the metabolic pathways associated with cholesterol were then analyzed. Both liver triglyceride and cholesterol contents were significantly increased in mice fed an FF/HS diet. Activation of fatty acid synthesis driven by the activation of sterol regulatory element binding protein (SREBP)-1c resulted in the increased liver triglycerides. The augmented cholesterol content in the liver could not be explained by an increased cholesterol synthesis, which was decreased by the FF/HS diet. HMG-CoA reductase protein level was decreased in mice fed an FF/HS diet. We found that the liver retained more cholesterol through a reduced excretion of bile acids, a reduced fecal cholesterol excretion, and an increased cholesterol uptake from plasma lipoproteins. Very low-density lipoproteintriglyceride and -cholesterol secretion were increased in mice fed an FF/HS diet, which led to hypertriglyceridemia and hypercholesterolemia in Ldlr-/- mice, a model that exhibits a more human like lipoprotein profile. These findings suggest that dietary cholesterol intake and cholesterol synthesis rates cannot only explain the hypercholesterolemia associated with NAFLD, and that the control of fatty acid synthesis should be considered for the management of dyslipidemia.